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Updated: May 7, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Bone morphogenetic proteins protect pulmonary microvascular endothelial cells from apoptosis by upregulating
Mariana Ciumas1, Mélanie Eyries, Odette Poirier
1From the UMR_S 956; Univ Paris 06 (UPMC); Institut National de la Santé et de la Recherche Médicale (INSERM), F-75013, Paris (M.C., M.E., O.P., S.M., F.D., K.M., S.N., F.S.); ICAN Institute for Cardiometabolism and Nutrition, Paris, France (M.E., O.P., S.M., F.D., S.N., F.S.); and UMR_S 999; INSERM; Univ Paris-Sud; LabEx LERMIT, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson, France (N.G.).
Objective:
To investigate the role of bone morphogenetic proteins (BMPs) on α-B-crystallin (CRYAB) expression and its physiological consequences on endothelial cells (ECs).
Approach And Results:
We report that the gene encoding for the small heat shock protein, CRYAB, is a transcriptional target of the BMP signaling pathway. We demonstrate that CRYAB expression is upregulated strongly by BMPs in an EC line and in human lung microvascular ECs and human umbilical vein ECs. We show that BMP signals through the BMPR2-ALK1 pathway to upregulate CRYAB expression through a transcriptional indirect mechanism involving Id1. We observed that the known antiapoptotic effect of the BMPs is, in part, because of the upregulation of CRYAB expression in EC. We also show that cryab is downregulated in vivo, in a mouse model of pulmonary arterial hypertension induced by chronic hypoxia where the BMP pathway is downregulated.
Conclusions:
We demonstrate a cross-talk between BMPs and CRYAB and a major effect of this regulatory interaction on resistance to apoptosis.
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